This study seeks to evaluate, by the use of an infant primate model, the hypothesis that the Sudden Infant Death Syndrome, (S.I.D.S.), does not necessarily involve a precipitous series of terminal events without antecedent pathology, but that victims of this disorder might be characterized by predisposing physiologic states, particularly chronic hypoxemia resulting from deficient ventilatory performance. Chronic hypoxemic states have been induced in infant monkeys by sustained exposure to depressed oxygen levels in a closed-system incubator. Additional animals will be made hypoxemic by production of diffuse ischemic lesions of the brainstem to interfere with ventilatory regulation. Others will be subjected to antenatal/perinatal hypoxemia by hypotensive reduction of placental circulation and cesarean delivery into an oxygen deficient environment. Using respiratory function measures and blood-gas analysis, the infants are compared with a control population with respect to adequacy of respiratory control, including basal respiratory function, response to altered composition of breathing gas and characteristics of laryngeal reflexes. Tissues are prepared for light microscopy and examined quantitatively for indices of chronic hypoxemia.